Evaluation of interactive effects between temperature and air pollution on health outcomes

Abstract

A large number of studies have shown that both temperature and air pollution (eg, particulate

matter and ozone) are associated with health outcomes. So far, it has received limited

attention whether air pollution and temperature interact to affect health outcomes. A few

studies have examined interactive effects between temperature and air pollution, but produced

conflicting results. This thesis aimed to examine whether air pollution (including ozone and

particulate matter) and temperature interacted to affect health outcomes in Brisbane, Australia

and 95 large US communities.

In order to examine the consistency across different cities and different countries, we used

two datasets to examine interactive effects of temperature and air pollution. One dataset was

collected in Brisbane City, Australia, during 1996-2000. The dataset included air pollution

(PM10, ozone and nitrogen dioxide), weather conditions (minimum temperature, maximum

temperature, relative humidity and rainfall) and different health outcomes. Another dataset

was collected from the 95 large US communities, which included air pollution (ozone was

used in the thesis), weather conditions (maximum temperature and dew point temperature)

and mortality (all non-external cause mortality and cardiorespiratory mortality).

Firstly, we used three parallel time-series models to examine whether maximum temperature

modified PM10 effects on cardiovascular hospital admissions (CHA), respiratory hospital

admissions (RHA), cardiovascular emergency visits (CEV), respiratory emergency visits

(REV), cardiovascular mortality (CM) and non-external cause mortality (NECM), at lags of

0-2 days in Brisbane. We used a Poisson generalized additive model (GAM) to fit a bivariate

model to explore joint response surfaces of both maximum temperature and particulate matter

less than 10 μm in diameter (PM10) on individual health outcomes at each lag. Results show

that temperature and PM10 interacted to affect different health outcomes at various lags. Then,

we separately fitted non-stratification and stratification GAM models to quantify the

interactive effects. In the non-stratification model, we examined the interactive effects by

including a pointwise product for both temperature and the pollutant. In the stratification

model, we categorized temperature into two levels using different cut-offs and then included

an interactive term for both pollutant and temperature. Results show that maximum

temperature significantly and positively modified the associations of PM10 with RHA, CEV,

REV, CM and NECM at various lags, but not for CHA.

Then, we used the above Poisson regression models to examine whether PM10 modified the

associations of minimum temperature with CHA, RHA, CEV, REV, CM and NECM at lags

of 0-2 days. In this part, we categorized PM10 into two levels using the mean as cut-off to fit

the stratification model. The results show that PM10 significantly modified the effects of

temperature on CHA, RHA, CM and NECM at various lags. The enhanced adverse

temperature effects were found at higher levels of PM10, but there was no clear evidence for

synergistic effects on CEV and REV at various lags. Three parallel models produced similar

results, which strengthened the validity of these findings.

Thirdly, we examined whether there were the interactive effects between maximum

temperature and ozone on NECM in individual communities between April and October,

1987-2000, using the data of 60 eastern US communities from the National Morbidity,

Mortality, and Air Pollution Study (NMMAPS). We divided these communities into two

regions (northeast and southeast) according to the NMMAPS study. We first used the

bivariate model to examine the joint effects between temperature and ozone on NECM in

each community, and then fit a stratification model in each community by categorizing

temperature into three levels. After that, we used Bayesian meta-analysis to estimate overall

effects across regions and temperature levels from the stratification model. The bivariate

model shows that temperature obviously modified ozone effects in most of the northeast

communities, but the trend was not obviously in the southeast region. Bayesian meta-analysis

shows that in the northeast region, a 10-ppb increment in ozone was associated with 2.2%

(95% posterior interval [PI]: 1.2%, 3.1 %), 3.1% (95% PI: 2.2%, 3.8 %) and 6.2 % (95% PI:

4.8%, 7.6 %) increase in mortality for low, moderate and high temperature levels, respectively,

while in the southeast region, a 10-ppb increment in ozone was associated with 1.1% (95% PI:

-1.1%, 3.2 %), 1.5% (95% PI: 0.2%, 2.8%) and 1.3% (95% PI: -0.3%, 3.0 %) increase in

mortality.

In addition, we examined whether temperature modified ozone effects on cardiovascular

mortality in 95 large US communities between May and October, 1987-2000 using the same

models as the above. We divided the communities into 7 regions according to the NMMAPS

study (Northeast, Industrial Midwest, Upper Midwest, Northwest, Southeast, Southwest and

Southern California). The bivariate model shows that temperature modified ozone effects in

most of the communities in the northern regions (Northeast, Industrial Midwest, Upper

Midwest, Northwest), but such modification was not obvious in the southern regions

(Southeast, Southwest and Southern California). Bayesian meta-analysis shows that

temperature significantly modified ozone effects in the Northeast, Industrial Midwest and

Northwest regions, but not significant in Upper Midwest, Southeast, Southwest and Southern

California. Nationally, temperature marginally positively modified ozone effects on

cardiovascular mortality. A 10-ppb increment in ozone was associated with 0.4% (95%

posterior interval [PI]: -0.2, 0.9 %), 0.3% (95% PI: -0.3%, 1.0%) and 1.6% (95% PI: 4.8%,

7.6%) increase in mortality for low, moderate and high temperature levels, respectively. The

difference of overall effects between high and low temperature levels was 1.3% (95% PI: -

0.4%, 2.9%) in the 95 communities.

Finally, we examined whether ozone modified the association between maximum temperature

and cardiovascular mortality in 60 large eastern US communities during the warmer days,

1987-2000. The communities were divided into the northeast and southeast regions. We

restricted the analyses to the warmer days when temperature was equal to or higher than the

median in each community throughout the study period. We fitted a bivariate model to

explore the joint effects between temperature and ozone on cardiovascular mortality in

individual communities and results show that in general, ozone positively modified the

association between temperature and mortality in the northeast region, but such modification

was not obvious in the southeast region. Because temperature effects on mortality might

partly intermediate by ozone, we divided the dataset into four equal subsets using quartiles as

cut-offs. Then, we fitted a parametric model to examine the associations between temperature

and mortality across different levels of ozone using the subsets. Results show that the higher

the ozone concentrations, the stronger the temperature-mortality associations in the northeast

region. However, such a trend was not obvious in the southeast region.

Overall, this study found strong evidence that temperature and air pollution interacted to

affect health outcomes. PM10 and temperature interacted to affect different health outcomes at

various lags in Brisbane, Australia. Temperature and ozone also interacted to affect NECM

and CM in US communities and such modification varied considerably across different

regions. The symmetric modification between temperature and air pollution was observed in

the study. This implies that it is considerably important to evaluate the interactive effect while

estimating temperature or air pollution effects and further investigate reasons behind the

regional variability.